Cells of all living organisms possess topoisomerases to resolve the topological problems associated with DNA supercoiling during various cellular processes (e.g. replication, transcription, repair).1 There are two major families of topoisomerases: type I and type II. Topisomerase type I (Top1) relaxes both positively and negatively supercoiled DNA via reversible single-strand nicks.2 Top1 forms a covalent link with the 3′-oxygen atom of DNA.3 The free 5′-end is then allowed to rotate about the intact strand, thus relieving tension. Once supercoils are removed, the broken DNA strand is re-ligated and the Top1 released.4 The importance of Top1 for DNA replication and cell division has made it an attractive drug target for anticancer therapy.5, 6 Camptothecin (CPT, 1), a natural product isolated from the Chinese tree Camptotheca acuminata, was the first small molecule to be identified as a Top1 inhibitor (Compound List 1). Topotecan and irinotecan, two clinically relevant analogues of CPT, have previously been described, along with other indenoisoquinolines,12-19 including an indenoisoquinoline discovered during the total synthesis of nitidine chloride.7, 8 Interest in indenoisoquinolines was increased by the observation that, despite displaying a similar cytotoxicity profile and ability to inhibit Top1 to that of CPT, the indenoisoquinolines lack the reportedly metabolically unstable lactone ring present in camptothecins.9, 10 The synthetic Top1 inhibitor topovale (6) has also been previously reported21. Cocrystallization of an indenoisoquinoline with Top1-DNA cleavage complex followed by X-ray crystallographic studies of the co-crystals was used to support the proposed molecular mechanism of Top1 inhibition by indenoisoquinolines.20 Without being bound by theory, it is believed that these molecules function by stabilizing the covalent Top1-DNA cleavage complex and preventing the re-ligation step. Prevention of the re-ligation step reportedly results in enhanced formation of persistent DNA breaks that eventually result in cell death.11 
Described herein are dibenzonaphthyridine compounds. In one illustrative embodiment, these compounds are dibenzo[c,h][1,6]naphthyridines. In another embodiment, these compounds posses a naphthyridinedione structure. In another illustrative embodiment, the compounds herein are dibenzo[c,h][1,6]naphthyridinediones and chlorodibenzo[c,h][1,6]naphthyridinones. It has been discovered that compounds described herein possess Top1 inhibiting properties. In addition, it has been discovered that compounds described herein are cytotoxic. In another embodiment, compounds are described herein that possess Top1 inhibitory activities with low micromolar to submicromolar cytotoxicity GI50 values. In another embodiment, this Top1 inhibition by the compounds herein leads to cell death. In another embodiment, compounds are described herein that possess different or unique DNA cleavage site selectivities compared to CPT and/or indenoisoquinolines. In another embodiment, compounds are described herein that exhibit potent antitumor activities in cancer cell lines. In another embodiment, compounds are described herein that exhibit antiproliferative properties. It is to be understood that the compounds and compositions disclosed herein can be used to control the growth of non-cancer cells that are over proliferating. In another embodiment, described herein are synthetic processes for preparation of the dibenzonaphthyridine compounds. In one aspect, these synthetic routes are efficient and scalable. In another aspect, the synthetic processes described herein may be used for the introduction of a variety of chemically sensitive functional groups into the naphthyridinedione structure. In another embodiment, described herein are pharmaceutical compositions and formulations comprising the dibenzonaphthyridine compounds. In another embodiment, described herein are methods for the use of the dibenzonaphthyridine compounds in the treatment and/or prevention of cancer.